We have assessed the clinical growth index as an indicator of tumour growth rate in 50 patients with a vestibular schwannoma. Clinical growth index was calculated by measuring the length of history and dividing it by the maximum tumour diameter. Total tumour volumes were also measured from all MRI examinations and an effective tumour volume doubling time was calculated. Radiological growth measurements demonstrated involution in 10/50 patients. The median volume doubling time was 1.65 years (range 20.9-46.3 months, skewness 1.72 years). The median clinical growth index was 0.030 cm per month (range 0-0.270 cm per month, skewness 2.398). There was no significant correlation between volume doubling time and clinical growth index. Identification of rapidly growing tumours with clinical growth index >0.025 cm/month had a positive predictive value of 61%, negative predictive value of 48%, false-positive rate of 30% and false-negative rate of 52%. In conclusion, we have shown that the growth rate of vestibular schwannoma is not related to the clinical growth index and we recommend that this measure should be abandoned in the clinical management of patients where conservative management regimes are being considered.
Background: Unilateral sporadic vestibular schwannomas (USVS) are caused by inactivating somatic mutations of both alleles of the neurofibromatosis 2 (NF2) tumor suppressor gene. Unilateral sporadic vestibular schwannomas have a widely-varying growth patterns whose causes are poorly understood. Objective: We examined the relationships between an index of USVS growth, and genetic abnormalities and pathological growth indices. Subjects and Methods: Single-strand conformational polymorphism analysis and heteroduplex methods were used to screen for mutations in all 17 exons of the NF2 gene in USVS from 63 patients. Loss of heterozygosity (LOH) analyses were also carried out. An index of USVS growth (clinical growth index, CGI) was calculated as maximum tumor diameter divided by duration of symptoms. The immunohistochemical growth indices were based on monoclonal antibodies to Ki-67 and another tumor cell proliferation marker (platelet-derived growth factor (PDGF)). Results: CGI was highly variable and did not significantly decrease with increasing age at diagnosis. Either somatic NF2 mutations or LOH was found in 88% of tumors. PDGF and Ki-67 increased significantly with increasing age at diagnosis, and PDGF was lower in tumors with LOH than in those without LOH. In multiple linear regression analysis, CGI was significantly higher in people with higher PDGF, after accounting for age at diagnosis and LOH. Conclusion: An index of USVS growth increases with increasing PDGF, after accounting for age and LOH.
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